+publisher:"University of Texas – Austin" +contributor:("Morrisett, Richard")

University of Texas – Austin

1. -4659-820X. Ethanol priming and its effects on consumption and accumbal plasticity.

Degree: MSin Pharmaceutical Sciences, Pharmaceutical sciences, 2015, University of Texas – Austin

► Alcohol abuse and dependence are major concerns in the United States because of their chronic, detrimental health effects and societal costs. The mesocorticolimbic pathway and… (more)

Subjects/Keywords: Ethanol; Accumbens; Operant; Self-administration

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APA (6^th Edition):

-4659-820X. (2015). Ethanol priming and its effects on consumption and accumbal plasticity. (Masters Thesis). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/34149

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Chicago Manual of Style (16^th Edition):

-4659-820X. “Ethanol priming and its effects on consumption and accumbal plasticity.” 2015. Masters Thesis, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/34149.

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MLA Handbook (7^th Edition):

-4659-820X. “Ethanol priming and its effects on consumption and accumbal plasticity.” 2015. Web. 27 Feb 2021.

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Author name may be incomplete

Vancouver:

-4659-820X. Ethanol priming and its effects on consumption and accumbal plasticity. [Internet] [Masters thesis]. University of Texas – Austin; 2015. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/34149.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Council of Science Editors:

-4659-820X. Ethanol priming and its effects on consumption and accumbal plasticity. [Masters Thesis]. University of Texas – Austin; 2015. Available from: http://hdl.handle.net/2152/34149

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

University of Texas – Austin

2. Wolfe, Sarah Anne. Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity.

Degree: PhD, Cellular and Molecular Biology, 2017, University of Texas – Austin

URL: http://dx.doi.org/10.26153/tsw/2231

► Alcohol Use Disorder (AUD) and Major Depressive Disorder (MDD) are two widespread and debilitating disorders that share a high rate of comorbidity with the presence… (more)

▼ Alcohol Use Disorder (AUD) and Major Depressive Disorder (MDD) are two widespread and debilitating disorders that share a high rate of comorbidity with the presence of either disorder doubling the risk of developing the other. Despite their prevalence, few treatments are available to individuals with comorbid AUD and MDD. Both alcohol and antidepressants promote lasting neuroadaptive changes in synapses and dendrites. With alcohol these changes may provide relief from depressive symptoms, and the initial use of alcohol may be a form of self-medication for individuals with MDD, suggesting ethanol may have antidepressant properties underlying similarities in neurobiological abnormalities. However, the synaptic pathways that are shared by alcohol and antidepressants are unknown. This study aims to identify why acute exposure to ethanol produced lasting antidepressant and anxiolytic behaviors. To understand the functional basis of these behaviors, a molecular pathway activated by rapid antidepressants was investigated. Here ethanol, like rapid antidepressants, altered γ-aminobutyric acid type B receptor (GABA [subscript B] R) expression and signaling, to increase dendritic calcium. New GABA [subscript B] Rs were synthesized in response to ethanol treatment, requiring fragile-X mental retardation protein (FMRP). Ethanol-dependent changes in GABA [subscript B] R expression, dendritic signaling, and antidepressant efficacy were absent in Fmr1-knockout (KO) mice. These findings indicate that FMRP is an important regulator of protein synthesis following acute alcohol exposure, and provided a molecular basis for the antidepressant efficacy of acute ethanol exposure. We identify alterations on a global scale with acute alcohol and antidepressant by sequencing the synaptic transcriptome. We identified parallel alterations in exon usage with acute alcohol and antidepressant treatment. These shared differentially expressed exons may give rise to isoforms and proteins with altered function or localization in the synapse. Some of these differentially expressed exons were identified in genes known to have alternative isoforms with AUD and MDD. These data implicate alternative splicing and isoform expression in the acute antidepressant-like effects of ethanol and the development of comorbid alcohol and depression. Understanding the molecular basis for comorbidity may aid in development of treatment options for afflicted individuals with dual disorders, as well as explore the mechanism for the initiation of addiction with acute exposure to alcohol Advisors/Committee Members: Harris, R. Adron (advisor), Raab-Graham, Kimberly F. (advisor), Golding, Nace (committee member), Morrisett, Richard (committee member), Macdonald, Paul (committee member).

Subjects/Keywords: Alcohol use disorder; Major depressive disorder; Ethanol; Rapid antidepressants; FMRP; GABABR; Ro 25-6981; RNA-sequencing; Synaptoneurosomes; Exon usage

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wolfe, S. A. (2017). Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://dx.doi.org/10.26153/tsw/2231

Chicago Manual of Style (16^th Edition):

Wolfe, Sarah Anne. “Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity.” 2017. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://dx.doi.org/10.26153/tsw/2231.

MLA Handbook (7^th Edition):

Wolfe, Sarah Anne. “Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity.” 2017. Web. 27 Feb 2021.

Vancouver:

Wolfe SA. Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2017. [cited 2021 Feb 27]. Available from: http://dx.doi.org/10.26153/tsw/2231.

Council of Science Editors:

Wolfe SA. Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity. [Doctoral Dissertation]. University of Texas – Austin; 2017. Available from: http://dx.doi.org/10.26153/tsw/2231

University of Texas – Austin

3. Renteria, Rafael III. Synaptic encoding of in vivo ethanol experience in the nucleus accumbens.

Degree: PhD, Neuroscience, 2015, University of Texas – Austin

URL: http://hdl.handle.net/2152/31598

► The nucleus accumbens (NAc) is a critical component of the brain reward system and neuroadaptations in the NAc are thought to underlie the development and… (more)

▼ The nucleus accumbens (NAc) is a critical component of the brain reward system and neuroadaptations in the NAc are thought to underlie the development and persistence of addiction. The NAc is composed of two subregions, the core and shell, in which medium spiny neurons (MSNs) are the primary cell type. There are two distinct subtypes of MSNs in the NAc depending on the dopamine receptor expression: D1 dopamine receptor expressing (D1+) MSNs and D2 dopamine receptor expressing MSNs (D1-). We conducted whole-cell patch clamp recordings using transgenic mice to selectively record from D1+ and D1- MSNs in the NAc and found that chronic intermittent ethanol (CIE) vapor exposure resulted in cell type specific alterations in the intrinsic properties and expression of plasticity. To detect changes in plasticity of AMPA receptor (AMPAR) mediated currents we used a well described form of NMDAR-dependent long-term depression (LTD) that is induced by pairing low frequency stimulation with postsynaptic depolarization. Similar to previous findings from our lab we found that LTD was expressed exclusively in D1+ MSNs of ethanol naïve mice. In slices prepared from CIE treated mice, the induction protocol instead resulted in long-term potentiation (LTP) in D1+ MSNs. The expression of LTP in D1+ MSNs was accompanied by an increase in excitability as well as an increase in the frequency of spontaneous EPSCs. Interestingly, CIE exposure uncovered the expression of LTD in D1- MSNs. To further our understanding as to how these neuroadaptations contribute to maladaptive ethanol drinking behaviors we used CIE vapor exposure to induce an increase in voluntary ethanol consumption. Electrophysiological experiments were conducted in the core and shell to determine if excitatory signaling and plasticity is differentially modulated between the two subregions. CIE induced an increase in ethanol drinking and resulted in the long-lasting disruption of LTD in D1+ MSNs of the NAc shell with no changes in the core. In addition we found that AMPAR conductance was significantly reduced at positive holding potentials suggesting the presence of GluA2-lacking AMPARs. These findings may constitute important neuroadaptations that underlie alcohol dependence and excessive alcohol consumption. Advisors/Committee Members: Morrisett, Richard A. (advisor), Gonzales, Rueben A (committee member), Harris, Robert A (committee member), Golding, Nace L (committee member), Morikawa, Hitoshi (committee member).

Subjects/Keywords: Plasticity; Ethanol

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APA (6^th Edition):

Renteria, R. I. (2015). Synaptic encoding of in vivo ethanol experience in the nucleus accumbens. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/31598

Chicago Manual of Style (16^th Edition):

Renteria, Rafael III. “Synaptic encoding of in vivo ethanol experience in the nucleus accumbens.” 2015. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/31598.

MLA Handbook (7^th Edition):

Renteria, Rafael III. “Synaptic encoding of in vivo ethanol experience in the nucleus accumbens.” 2015. Web. 27 Feb 2021.

Vancouver:

Renteria RI. Synaptic encoding of in vivo ethanol experience in the nucleus accumbens. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2015. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/31598.

Council of Science Editors:

Renteria RI. Synaptic encoding of in vivo ethanol experience in the nucleus accumbens. [Doctoral Dissertation]. University of Texas – Austin; 2015. Available from: http://hdl.handle.net/2152/31598

University of Texas – Austin

4. Zandy, Shannon Laine. Effects of opioid antagonism on operant ethanol self-administration in adolescence and characterization of extracellular GABA in the ventral tegmental area.

Degree: PhD, Pharmaceutical sciences, 2016, University of Texas – Austin

URL: http://hdl.handle.net/2152/46447

► The endogenous opioid peptide system is hypothesized to be involved in ethanol self-administration and relapse behaviors. Naltrexone, a nonselective opioid antagonist, is an approved medication… (more)

▼ The endogenous opioid peptide system is hypothesized to be involved in ethanol self-administration and relapse behaviors. Naltrexone, a nonselective opioid antagonist, is an approved medication for alcohol use disorder which has been shown to decrease drinking in adult animal models and select clinical populations, but little is known about the efficacy of naltrexone in animal models that begin drinking ethanol in adolescence. Therefore, we investigated the effects of systemic naltrexone administration in an adolescent rat model of operant ethanol self-administration. We found that naltrexone significantly reduced ethanol intake and motivation to obtain ethanol in adolescent and adult rats. Following a period of abstinence, naltrexone also significantly reduced “relapse” to alcohol seeking in both age groups. These results extend findings that naltrexone is effective at reducing ethanol intake to an adolescent animal model and support opioid antagonism as a treatment strategy for decreasing problem drinking in late adolescents and young adults. One potential mechanism underlying the effects of opioid receptor blockade on ethanol self-administration implicates γ-aminobutyric acid (GABA) neurons within the ventral tegmental area (VTA). Inhibitory signaling in the VTA is involved in the mechanism of action of many drugs of abuse yet there are few studies measuring extracellular GABA concentration in this region. Therefore, the remaining experiments focused on developing methods to quantify extracellular GABA in the VTA. We first describe a novel, sensitive fluorescence method to quantify GABA concentration using high performance liquid chromatography (HPLC) of an ophthalaldehyde/sulfite derivative, previously reported to produce low fluorescence not suitable for in vivo microdialysis applications. Next, we used quantitative microdialysis under transient conditions to characterize basal extracellular GABA concentration and the influence of uptake mechanisms in the VTA. Our results show that inhibition of GABA uptake significantly increased extracellular GABA concentration and reduced in vivo extraction fraction of the probe. Reduced in vivo extraction fraction caused significant underestimation of the increase in extracellular GABA by conventional microdialysis. Together, these results establish the foundation for future studies to investigate the regulation of extracellular GABA concentration and uptake mechanisms in the VTA in mediating the effects of ethanol, opioid antagonism and associated drug-related behaviors. Advisors/Committee Members: Gonzales, Rueben Anthony (advisor), Harris, Robert A (committee member), Marinelli, Michela (committee member), Morikawa, Hitoshi (committee member), Morrisett, Richard A (committee member).

Subjects/Keywords: Adolescence; Ethanol; GABA; Microdialysis; Naltrexone; Nipecotic acid; No net flux; VTA

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APA (6^th Edition):

Zandy, S. L. (2016). Effects of opioid antagonism on operant ethanol self-administration in adolescence and characterization of extracellular GABA in the ventral tegmental area. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/46447

Chicago Manual of Style (16^th Edition):

Zandy, Shannon Laine. “Effects of opioid antagonism on operant ethanol self-administration in adolescence and characterization of extracellular GABA in the ventral tegmental area.” 2016. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/46447.

MLA Handbook (7^th Edition):

Zandy, Shannon Laine. “Effects of opioid antagonism on operant ethanol self-administration in adolescence and characterization of extracellular GABA in the ventral tegmental area.” 2016. Web. 27 Feb 2021.

Vancouver:

Zandy SL. Effects of opioid antagonism on operant ethanol self-administration in adolescence and characterization of extracellular GABA in the ventral tegmental area. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2016. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/46447.

Council of Science Editors:

Zandy SL. Effects of opioid antagonism on operant ethanol self-administration in adolescence and characterization of extracellular GABA in the ventral tegmental area. [Doctoral Dissertation]. University of Texas – Austin; 2016. Available from: http://hdl.handle.net/2152/46447

University of Texas – Austin

5. Vena, Ashley. The pharmacological effects of acute ethanol on catecholamines in the medial prefrontal cortex and dorsal striatum.

Degree: PhD, Pharmaceutical sciences, 2016, University of Texas – Austin

URL: http://hdl.handle.net/2152/46147

► The dorsal striatum and the medial prefrontal cortex are part of a neurocircuitry that is affected by acute and chronic drug use. In the present… (more)

▼ The dorsal striatum and the medial prefrontal cortex are part of a neurocircuitry that is affected by acute and chronic drug use. In the present studies, we sought to characterize the pharmacological effects of ethanol on extracellular catecholamine concentrations in the dorsal striatum and medial prefrontal cortex. To this end, we utilized two different routes of administration to quantify ethanol’s actions. We performed in vivo microdialysis in adult, male Long Evans rats as they received single or repeated intravenous infusions of ethanol. Following infusion of a 1-g/kg dose of ethanol, we observed no significant effects on extracellular dopamine in either the dorsomedial or dorsolateral striatum, but in a separate group of animals, we observed significant stimulation of extracellular norepinephrine in the medial prefrontal cortex. However, following a cumulative intravenous dosing protocol, we observed a gradual ramping up of tonic dopamine activity in the dorsal striatal subregions, which was more robust in the dorsomedial striatum. Subsequently, we performed in vivo microdialysis in separate groups of rats during an operant self-administration session to quantify the time course of extracellular dopamine and norepinephrine in the medial prefrontal cortex. In the seven operant sessions prior to the microdialysis test session, each group of rats had been assigned to a separate treatment group: one that received a sweetened ethanol solution, one that received a sucrose solution, and a handling control group that did not receive any drinking solutions. In the ethanol-experienced animals, we report a reduction in basal dopamine and norepinephrine in the medial prefrontal cortex, relative to control groups. However, there were no significant differences in the temporal profile of extracellular norepinephrine across the three treatment groups. These studies demonstrate that limited voluntary ethanol consumption appears to be sufficient to alter tonic catecholamine signaling in the medial prefrontal cortex. Additionally, we conclude that central catecholamine signaling pathways are a target for ethanol. Advisors/Committee Members: Gonzales, Rueben Anthony (advisor), Dominguez, Juan (committee member), Harris, Adron (committee member), Duvauchelle, Christine (committee member), Morrisett, Richard (committee member).

Subjects/Keywords: Ethanol; Striatum; Prefrontal cortex; Dopamine; Norepinephrine; Catecholamines; Self-administration; Pharmacology

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APA (6^th Edition):

Vena, A. (2016). The pharmacological effects of acute ethanol on catecholamines in the medial prefrontal cortex and dorsal striatum. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/46147

Chicago Manual of Style (16^th Edition):

Vena, Ashley. “The pharmacological effects of acute ethanol on catecholamines in the medial prefrontal cortex and dorsal striatum.” 2016. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/46147.

MLA Handbook (7^th Edition):

Vena, Ashley. “The pharmacological effects of acute ethanol on catecholamines in the medial prefrontal cortex and dorsal striatum.” 2016. Web. 27 Feb 2021.

Vancouver:

Vena A. The pharmacological effects of acute ethanol on catecholamines in the medial prefrontal cortex and dorsal striatum. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2016. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/46147.

Council of Science Editors:

Vena A. The pharmacological effects of acute ethanol on catecholamines in the medial prefrontal cortex and dorsal striatum. [Doctoral Dissertation]. University of Texas – Austin; 2016. Available from: http://hdl.handle.net/2152/46147

University of Texas – Austin

6. -3954-6468. The role of monocyte chemoattractant protein-1 on operant ethanol self-administration in Long-Evans rats.

Degree: PhD, Psychology, 2015, University of Texas – Austin

URL: http://hdl.handle.net/2152/33354

► The neuroimmune system can exert a powerful influence over behavior, and evidence is mounting that the neuroimmune system can influence the intake of drugs of… (more)

▼ The neuroimmune system can exert a powerful influence over behavior, and evidence is mounting that the neuroimmune system can influence the intake of drugs of abuse. Insight into the interaction between drugs of abuse and the neuroimmune system will teach us more about the inner workings of the brain and can lead to new treatment options for addiction. Previous research has demonstrated that alcoholics have elevated levels of immune signaling molecules. My dissertation project demonstrated that elevating immune signaling molecules in the brain can directly increase ethanol consumption. A variety of cytokines are elevated in human alcoholics and animal models of ethanol dependence. However, recent research has suggested that monocyte chemoattractant protein -1 (MCP-1) is particularly important. Researchers have found elevated levels of MCP-1 in the brains of human alcoholics, in animal brains after chronic exposure to ethanol, and in brain slices exposed to ethanol. Also, MCP-1 or MCP-1 receptor (CCR2) knockout mice had a significant reduction in ethanol consumption and a reduced preference for ethanol. My goal was to clarify if MCP-1 signaling could increase ethanol intake. Generally speaking, I accomplished this by increasing the amount of MCP-1 signaling in the brain and then measuring ethanol drinking behavior. I infused MCP-1 into the cerebral ventricles of rodents for 4 weeks and measured their ethanol intake for those 4 weeks as well as 4 additional weeks. There was a significant interaction between dose of MCP-1 and ethanol consumed across the first 4 weeks (while pumps were flowing) and across the 8-week experiment. Animals receiving the highest dose of MCP-1 (2 µg/day) were the highest consumers of ethanol during weeks 3 through 8. My second goal was to determine how the modulation of brain MCP-1 signaling could influence drinking behavior in ethanol-dependent rodents. I made progress toward this goal by reliably reaching target BAC’s in rodents through the use of ethanol vapor inhalation chambers, but I did not reach the point of inducing dependence or modulating MCP-1. The neuroimmune system seems to be paramount in the progressive loss of control over drug intake seen in drug addiction and presents a potential route for the treatment of addiction. The results of my experiments support this hypothesis by providing evidence that neuroimmune signaling can increase ethanol consumption, show that MCP-1 signaling is critical in this phenomenon, and identify MCP-1 signaling as a strong candidate for investigating the therapeutic potential of neuroimmune signaling for alcohol use disorders. Advisors/Committee Members: Gonzales, Rueben Anthony (advisor), Harris, R. Adron (committee member), Morrisett, Richard (committee member), Schallert, Timothy (committee member), Dominguez, Juan (committee member), Wright, Casey (committee member).

Subjects/Keywords: Alcoholism; Neuropharmacology

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APA (6^th Edition):

-3954-6468. (2015). The role of monocyte chemoattractant protein-1 on operant ethanol self-administration in Long-Evans rats. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/33354

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Author name may be incomplete

Chicago Manual of Style (16^th Edition):

-3954-6468. “The role of monocyte chemoattractant protein-1 on operant ethanol self-administration in Long-Evans rats.” 2015. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/33354.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

MLA Handbook (7^th Edition):

-3954-6468. “The role of monocyte chemoattractant protein-1 on operant ethanol self-administration in Long-Evans rats.” 2015. Web. 27 Feb 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

-3954-6468. The role of monocyte chemoattractant protein-1 on operant ethanol self-administration in Long-Evans rats. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2015. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/33354.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Council of Science Editors:

-3954-6468. The role of monocyte chemoattractant protein-1 on operant ethanol self-administration in Long-Evans rats. [Doctoral Dissertation]. University of Texas – Austin; 2015. Available from: http://hdl.handle.net/2152/33354

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

7. Jeanes, Zachary Marvin. Mesocorticolimbic adaptations in synaptic plasticity underlie the development of alcohol dependence.

Degree: PhD, Pharmacy, 2012, University of Texas – Austin

URL: http://hdl.handle.net/2152/22178

► Synaptic alterations in the nucleus accumbens (NAc) are crucial for the aberrant reward-associated learning that forms the foundation of drug dependence. Glutamatergic synaptic plasticity in… (more)

▼ Synaptic alterations in the nucleus accumbens (NAc) are crucial for the aberrant reward-associated learning that forms the foundation of drug dependence. Glutamatergic synaptic plasticity in the NAc has been implicated in several behavioral responses to psychomotor stimulating agents, such as cocaine and amphetamine, yet no studies, at present, have investigated its modulation by ethanol. We demonstrated that both in vitro and in vivo ethanol treatment significantly disrupts normal synaptic functioning in medium spiny neurons (MSNs) of the NAc shell. Utilizing whole-cell voltage clamp recording techniques, synaptic conditioning (low frequency stimulation with concurrent postsynaptic depolarization) reliably depressed (NAc-LTD) AMPA-mediated excitatory postsynaptic currents (EPSCs). Acute ethanol exposure inhibited the depression of AMPA EPSCs differentially with increasing concentrations, but this inhibitory action of ethanol was reversed by a D1-like dopamine receptor agonist. When examined 24 hours following a single bout of in vivo chronic intermittent ethanol (CIE) vapor exposure, NAc-LTD was absent and instead synaptic potentiation (LTP) was reliably observed. We further investigated CIE-induced modulation of NAc-LTD by distinguishing between the two subpopulations of MSNs in the NAc, D1 receptor-expressing (D1+) and D2 receptor-expressing (D1-). We determined that NAc-LTD is expressed solely in D1+ but not D1- MSNs. In addition, 24 hours following a repeated regimen of in vivo CIE exposure NAc-LTD is completely occluded in D1+ MSNs, while D1- MSNs are able to express LTD. Complete recovery of normal synaptic plasticity expression in both D1+ and D1- MSNs does not occur until two weeks of withdrawal from CIE vapor exposure. To our knowledge, this is the first demonstration of a reversal in the cell type-specificity of synaptic plasticity in the NAc shell, as well as, the gradual recovery of the pre-drug exposure plasticity state following extended withdrawal. This study suggests that NAc-LTD is cell type-specific and highly sensitive to both acute and chronic ethanol exposure. We believe these observations also highlight the adaptability of NAc MSNs to the effects of long-term ethanol exposure. A change in these synaptic processes may constitute a neural adaptation that contributes to the induction and/or expression of alcohol dependence. Advisors/Committee Members: Morrisett, Richard A. (advisor).

Subjects/Keywords: Alcohol; Synaptic plasticity; Dependence

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APA (6^th Edition):

Jeanes, Z. M. (2012). Mesocorticolimbic adaptations in synaptic plasticity underlie the development of alcohol dependence. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/22178

Chicago Manual of Style (16^th Edition):

Jeanes, Zachary Marvin. “Mesocorticolimbic adaptations in synaptic plasticity underlie the development of alcohol dependence.” 2012. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/22178.

MLA Handbook (7^th Edition):

Jeanes, Zachary Marvin. “Mesocorticolimbic adaptations in synaptic plasticity underlie the development of alcohol dependence.” 2012. Web. 27 Feb 2021.

Vancouver:

Jeanes ZM. Mesocorticolimbic adaptations in synaptic plasticity underlie the development of alcohol dependence. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2012. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/22178.

Council of Science Editors:

Jeanes ZM. Mesocorticolimbic adaptations in synaptic plasticity underlie the development of alcohol dependence. [Doctoral Dissertation]. University of Texas – Austin; 2012. Available from: http://hdl.handle.net/2152/22178

8. Salinas, Armando. Central amygdala CART modulates ethanol withdrawal-induced anxiety.

Degree: PhD, Pharmacy, 2013, University of Texas – Austin

URL: http://hdl.handle.net/2152/27206

► Cocaine- and amphetamine-regulated transcript (CART), as its name implies, was initially identified as an upregulated transcript in response to psychostimulant administration. Consequently, it has been… (more)

▼ Cocaine- and amphetamine-regulated transcript (CART), as its name implies, was initially identified as an upregulated transcript in response to psychostimulant administration. Consequently, it has been posited to play a role in psychostimulant abuse and dependence. Spurred on by the finding that a polymorphism in the CART gene was associated with alcoholism, we initiated studies designed to elucidate the role of CART peptide in alcohol dependence. We first investigated the functional significance of CART peptide in alcohol dependence in vivo using a CART KO mouse. We found that CART KO mice had a significant decrease in ethanol consumption that could not be attributed to differences in total intake, taste perception, metabolism, or sensitivity to ethanol. In vitro we found that CART peptide facilitated NMDA receptor-mediated currents in central amygdala neurons. Given the emerging role of CART peptide in anxiety and stress, we decided to examine basal and stress-induced anxiety behaviors in CART KO mice. Under basal and acute stress conditions, CART KO mice did not differ in anxiety-like behaviors from WT mice; however, in response to a stressor, CART KO mice exhibited a potentiated corticosterone response. Using chronic intermittent ethanol exposure (CIE), we tested CART KO and WT mice for common signs of ethanol dependence including an escalation of volitional consumption and the presence of withdrawal-induced anxiety. We further investigated glutamatergic neuroadaptations within the central amygdala of CART KO and WT mice following CIE exposure and early withdrawal. CIE increased ethanol consumption and anxiety-like behaviors in mice of both genotypes but to a lower extent in CART KO mice. Electrophysiologically, CIE enhanced spontaneous excitatory postsynaptic currents in both genotypes and decreased the probability of presynaptic release in WT mice only. We believe that these electrophysiological neuroadaptations contribute to the development of ethanol dependence and may mediate withdrawal-induced anxiety behaviors. Overall, these studies indicate a role for CART peptide in alcohol dependence and specifically in modulating ethanol withdrawal-induced anxiety. Advisors/Committee Members: Morrisett, Richard A. (advisor).

Subjects/Keywords: CART; Anxiety; Alcoholism; Ethanol; Withdrawal; Amygdala; Addiction

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APA (6^th Edition):

Salinas, A. (2013). Central amygdala CART modulates ethanol withdrawal-induced anxiety. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/27206

Chicago Manual of Style (16^th Edition):

Salinas, Armando. “Central amygdala CART modulates ethanol withdrawal-induced anxiety.” 2013. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/27206.

MLA Handbook (7^th Edition):

Salinas, Armando. “Central amygdala CART modulates ethanol withdrawal-induced anxiety.” 2013. Web. 27 Feb 2021.

Vancouver:

Salinas A. Central amygdala CART modulates ethanol withdrawal-induced anxiety. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2013. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/27206.

Council of Science Editors:

Salinas A. Central amygdala CART modulates ethanol withdrawal-induced anxiety. [Doctoral Dissertation]. University of Texas – Austin; 2013. Available from: http://hdl.handle.net/2152/27206

University of Texas – Austin

9. Diaz, Laurea Marie. Dopamine and ethanol induced trafficking of viral mediated eGFP tagged dopamine D1 receptors in parasagittal explants.

Degree: PhD, Pharmacy, 2005, University of Texas – Austin

URL: http://hdl.handle.net/2152/1536

► The mesolimbic pathway has been implicated in the rewarding effects of drugs of abuse, and an important component of this pathway is the D1 dopamine… (more)

▼ The mesolimbic pathway has been implicated in the rewarding effects of drugs of abuse, and an important component of this pathway is the D1 dopamine receptor (D1DR). D1DRs desensitize upon agonist stimulation by several mechanisms, including a process involving receptor clustering and internalization. This process removes postsynaptic D1DRs and may be a neuroadaptive mechanism associated with addiction to drugs of abuse, including ethanol. We measured localization of D1DRs in viable nucleus accumbens (NAcc) neurons from parasagittal explants. A sindbis RNA virus was used to mediate the expression of D1DRs containing an enhanced green fluorescent protein (eGFP) tag in these explants. The effects of dopamine and ethanol on D1DR localization were measured by changes in fluorescence intensity using two-photon laser scanning microscopy. Two-dimensional images from z-stacks of virally infected neurons displayed stable and homogenous fluorescence throughout the neuronal soma and processes. Dopamine (100 uM, 30 min) significantly enhanced the greatest increase of maximum fluorescence intensity in distinct regions of interest (ROIs) by approximately 40% compared to control neurons in the absence of dopamine. Ethanol pretreatment significantly enhanced dopamine-induced clustering. Neurons exposed to dopamine (50 uM, 30 min) displayed receptor clustering only when pretreated with ethanol. Ethanol (50 and 100 mM, 30 min.) pretreatment followed by dopamine (50 uM, 30 min.) enhanced the greatest increase of maximum fluorescence intensity by 44±3 and 108±9%, respectively, while dopamine (50 uM, 30 min) in the absence of ethanol pretreatment showed no clustering with peak increases in maximum fluorescence intensity of only 3±2%. Ethanol (50 and 100 mM, 60 min) alone enhance the greatest increase of maximum fluorescence intensity by about 60% for both concentrations. Receptor clustering induced by dopamine, ethanol pretreatment of dopamine, or ethanol alone was partially blocked by the D1DR antagonist SCH 23390 (20 uM). These findings show that both dopamine and ethanol alter D1DR localization in NAcc neurons and suggest that a physical restructuring of D1DRs in this region may be involved in neuroadaptive mechanisms of ethanol action Advisors/Committee Members: Morrisett, Richard A. (advisor).

Subjects/Keywords: Dopamine – Receptors; Dopamine – Physiological effect; Alcohol – Physiological effect

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APA (6^th Edition):

Diaz, L. M. (2005). Dopamine and ethanol induced trafficking of viral mediated eGFP tagged dopamine D1 receptors in parasagittal explants. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/1536

Chicago Manual of Style (16^th Edition):

Diaz, Laurea Marie. “Dopamine and ethanol induced trafficking of viral mediated eGFP tagged dopamine D1 receptors in parasagittal explants.” 2005. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/1536.

MLA Handbook (7^th Edition):

Diaz, Laurea Marie. “Dopamine and ethanol induced trafficking of viral mediated eGFP tagged dopamine D1 receptors in parasagittal explants.” 2005. Web. 27 Feb 2021.

Vancouver:

Diaz LM. Dopamine and ethanol induced trafficking of viral mediated eGFP tagged dopamine D1 receptors in parasagittal explants. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2005. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/1536.

Council of Science Editors:

Diaz LM. Dopamine and ethanol induced trafficking of viral mediated eGFP tagged dopamine D1 receptors in parasagittal explants. [Doctoral Dissertation]. University of Texas – Austin; 2005. Available from: http://hdl.handle.net/2152/1536

University of Texas – Austin

10. Zhang, Tao. Dopamine D1-like receptor-mediated regulation of NMDA receptor sensitivity to ethanol in the nucleus accumbens.

Degree: PhD, Neuroscience, 2005, University of Texas – Austin

URL: http://hdl.handle.net/2152/2213

Subjects/Keywords: Methyl aspartate – Receptors; Dopamine – Physiological effect; Alcohol – Physiological effect

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APA (6^th Edition):

Zhang, T. (2005). Dopamine D1-like receptor-mediated regulation of NMDA receptor sensitivity to ethanol in the nucleus accumbens. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/2213

Chicago Manual of Style (16^th Edition):

Zhang, Tao. “Dopamine D1-like receptor-mediated regulation of NMDA receptor sensitivity to ethanol in the nucleus accumbens.” 2005. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/2213.

MLA Handbook (7^th Edition):

Zhang, Tao. “Dopamine D1-like receptor-mediated regulation of NMDA receptor sensitivity to ethanol in the nucleus accumbens.” 2005. Web. 27 Feb 2021.

Vancouver:

Zhang T. Dopamine D1-like receptor-mediated regulation of NMDA receptor sensitivity to ethanol in the nucleus accumbens. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2005. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/2213.

Council of Science Editors:

Zhang T. Dopamine D1-like receptor-mediated regulation of NMDA receptor sensitivity to ethanol in the nucleus accumbens. [Doctoral Dissertation]. University of Texas – Austin; 2005. Available from: http://hdl.handle.net/2152/2213

11. -5710-1123. Ethanol experience elicits circuit specific adaptations of ventral hippocampal-accumbens glutamatergic signaling.

Degree: PhD, Pharmaceutical Sciences, 2018, University of Texas – Austin

URL: http://hdl.handle.net/2152/63989

► The purpose of this study was to determine the effects of ethanol exposure and consumption on the expression of plasticity of D1 dopamine receptor expressing… (more)

Subjects/Keywords: Electrophysiology; Optogenetics; Nucleus accumbens; NAc; Ventral hippocampus; vHipp; Alcohol; Ethanol; CIE; 2BC; Ethanol vapor; Plasticity; LTD; NMDAR-LTD; CPAR; GluA2 lacking

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APA (6^th Edition):

-5710-1123. (2018). Ethanol experience elicits circuit specific adaptations of ventral hippocampal-accumbens glutamatergic signaling. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/63989

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Chicago Manual of Style (16^th Edition):

-5710-1123. “Ethanol experience elicits circuit specific adaptations of ventral hippocampal-accumbens glutamatergic signaling.” 2018. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/63989.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

MLA Handbook (7^th Edition):

-5710-1123. “Ethanol experience elicits circuit specific adaptations of ventral hippocampal-accumbens glutamatergic signaling.” 2018. Web. 27 Feb 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

-5710-1123. Ethanol experience elicits circuit specific adaptations of ventral hippocampal-accumbens glutamatergic signaling. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2018. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/63989.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Council of Science Editors:

-5710-1123. Ethanol experience elicits circuit specific adaptations of ventral hippocampal-accumbens glutamatergic signaling. [Doctoral Dissertation]. University of Texas – Austin; 2018. Available from: http://hdl.handle.net/2152/63989

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

12. McCracken, Lindsay Marie. A critical role for zinc in ethanol action at the glycine receptor.

Degree: PhD, Pharmacology, 2012, University of Texas – Austin

URL: http://hdl.handle.net/2152/ETD-UT-2012-05-4979

► Ethanol is a widely used drug, yet an understanding of its sites and mechanisms of action remains incomplete. Among the protein targets of ethanol are… (more)

▼ Ethanol is a widely used drug, yet an understanding of its sites and mechanisms of action remains incomplete. Among the protein targets of ethanol are glycine receptors (GlyRs). In addition to ethanol, zinc also modulates GlyR function. Although the individual effects of zinc and alcohols on GlyR function have been well studied, the combined effects of these agents have not been thoroughly examined. This project investigated the effects of zinc on alcohol action at the glycine receptor (GlyR). In Aim 1, the effects of zinc on ethanol modulation of GlyR function were tested and characterized in three GlyR [alpha] subunits ([alpha]1-3). Aim 2 explored a site of action for the augmenting effects of zinc on ethanol action at the GlyR. Mutant D80A GlyRs, which lack a zinc binding site (D80), were constructed and allowed us determine if this zinc binding site is important for the zinc/ethanol interactions that were observed in Aim 1. The effects of ethanol were reduced in mutant D80A GlyRs compared to wild type (WT). In addition, manipulating zinc levels in our buffers either by adding or chelating zinc did not change the magnitude of ethanol enhancement of mutant D80A GlyRs as it did in WT GlyRs suggesting that the D80 position is important for zinc modulation of ethanol action. Finally, Aim 3 extended the findings from Aims 1 and 2 by evaluating the effects of a GlyR point-mutation on alcohol consumption and other behavioral tests in mice. Glra1(D80A) knock-in mice provided an animal model for behavioral studies of zinc/ethanol interactions at the GlyR and showed decreased alcohol consumption and preference compared to their WT littermates. In addition, D80A KI mice had increased startle responses compared to their WT littermates. Other behavioral tests were also conducted including tests of ethanol motor incoordination and strychnine induced convulsions; there were no differences detected between KI and WT mice in these assays. Overall, our findings demonstrate that zinc is critical in determining the effects of ethanol at GlyRs and suggest that zinc signaling at the D80 position may be important for mediating the behavioral effects of ethanol action at GlyRs. Advisors/Committee Members: Harris, R. Adron (advisor), Gore, Andrea (committee member), Duvauchelle, Christine (committee member), Morrisett, Richard (committee member), Trudell, James (committee member).

Subjects/Keywords: Ethanol; Glycine receptors; Zinc

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APA (6^th Edition):

McCracken, L. M. (2012). A critical role for zinc in ethanol action at the glycine receptor. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/ETD-UT-2012-05-4979

Chicago Manual of Style (16^th Edition):

McCracken, Lindsay Marie. “A critical role for zinc in ethanol action at the glycine receptor.” 2012. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/ETD-UT-2012-05-4979.

MLA Handbook (7^th Edition):

McCracken, Lindsay Marie. “A critical role for zinc in ethanol action at the glycine receptor.” 2012. Web. 27 Feb 2021.

Vancouver:

McCracken LM. A critical role for zinc in ethanol action at the glycine receptor. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2012. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/ETD-UT-2012-05-4979.

Council of Science Editors:

McCracken LM. A critical role for zinc in ethanol action at the glycine receptor. [Doctoral Dissertation]. University of Texas – Austin; 2012. Available from: http://hdl.handle.net/2152/ETD-UT-2012-05-4979

13. Moorjani, Samira Gian. Directing cell migration by dynamic control of laminar streams.

Degree: PhD, Biomedical Engineering, 2010, University of Texas – Austin

URL: http://hdl.handle.net/2152/ETD-UT-2010-12-2146

► Interactions of cells with their chemical microenvironments are critical to many polarized processes, including differentiation, migration, and pathfinding. To investigate such cellular events, tools are… (more)

Subjects/Keywords: Microfluidics; Laminar streams; Neutrophil migration and chemotaxis; Chemical dosing; Chemical gradients; Laser-induced ablation; Laminar flow; Effector

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APA (6^th Edition):

Moorjani, S. G. (2010). Directing cell migration by dynamic control of laminar streams. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/ETD-UT-2010-12-2146

Chicago Manual of Style (16^th Edition):

Moorjani, Samira Gian. “Directing cell migration by dynamic control of laminar streams.” 2010. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/ETD-UT-2010-12-2146.

MLA Handbook (7^th Edition):

Moorjani, Samira Gian. “Directing cell migration by dynamic control of laminar streams.” 2010. Web. 27 Feb 2021.

Vancouver:

Moorjani SG. Directing cell migration by dynamic control of laminar streams. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2010. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/ETD-UT-2010-12-2146.

Council of Science Editors:

Moorjani SG. Directing cell migration by dynamic control of laminar streams. [Doctoral Dissertation]. University of Texas – Austin; 2010. Available from: http://hdl.handle.net/2152/ETD-UT-2010-12-2146

14. Li, Na, 1980 Oct. 2-. Binaural mechanism revealed with in vivo whole cell patch clamp recordings in the inferior colliculus.

Degree: PhD, Neuroscience, 2010, University of Texas – Austin

URL: http://hdl.handle.net/2152/ETD-UT-2010-12-2065

► Many cells in the inferior colliculus (IC) are excited by contralateral and inhibited by ipsilateral stimulation and are thought to be important for sound localization.… (more)

▼ Many cells in the inferior colliculus (IC) are excited by contralateral and inhibited by ipsilateral stimulation and are thought to be important for sound localization. These excitatory-inhibitory (EI) cells comprise a diverse group, even though they exhibit a common binaural response property. Previous extracellular studies proposed specific excitatory and/or inhibitory events that should be evoked by each ear and thereby generate each of the EI discharge properties. The proposals were inferences based on the well established response features of neurons in lower nuclei, the projections of those nuclei, their excitatory or inhibitory neurochemistry, and the changes in response features that occurred when inhibition was blocked. Here we recorded the inputs, the postsynaptic potentials, discharges evoked by monaural and binaural signals in EI cells with in vivo whole cell recordings from the inferior colliculus (IC) of awake bats. We also computed the excitatory and inhibitory synaptic conductances from the recorded sound evoked responses. First, we showed that a minority of EI cells either inherited their binaural property from a lower binaural nucleus or the EI property was created in the IC via inhibitory projections from the ipsilateral ear, features consistent with those observed in extracellular studies. Second, we showed that in a majority of EI cells ipsilateral signals evoked subthreshold EPSPs that behaved paradoxically in that EPSP amplitudes increased with intensity, even though binaural signals with the same ipsilateral intensities generated progressively greater spike suppressions. These ipsilateral EPSPs were unexpected since they could not have been detected with extracellular recordings. These additional responses suggested that the circuitry underlying EI cells was more complex than previously suggested. We also proposed the functional significance of ipsilaterally evoked EPSPs in responding to moving sound sources or multiple sounds. Third, by computing synaptic conductances, we showed the circuitry of the EI cells was even more complicated than those suggested by PSPs, and we also evaluated how the binaural property was produced by the contralateral and ipsilateral synaptic events. Advisors/Committee Members: Pollak, G. D. (George D.), 1942- (advisor), Huk, Alex (committee member), Priebe, Nicholas (committee member), Golding, Nace (committee member), Zakon, Harold (committee member), Morrisett, Richard (committee member).

Subjects/Keywords: Patch clamp recording; Inferior colliculus; Excitatory-inhibitory; Precedence effect; Sound localization; EI cells; Ipsilateral response; Binaural property

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APA (6^th Edition):

Li, Na, 1. O. 2. (2010). Binaural mechanism revealed with in vivo whole cell patch clamp recordings in the inferior colliculus. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/ETD-UT-2010-12-2065

Chicago Manual of Style (16^th Edition):

Li, Na, 1980 Oct 2-. “Binaural mechanism revealed with in vivo whole cell patch clamp recordings in the inferior colliculus.” 2010. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/ETD-UT-2010-12-2065.

MLA Handbook (7^th Edition):

Li, Na, 1980 Oct 2-. “Binaural mechanism revealed with in vivo whole cell patch clamp recordings in the inferior colliculus.” 2010. Web. 27 Feb 2021.

Vancouver:

Li, Na 1O2. Binaural mechanism revealed with in vivo whole cell patch clamp recordings in the inferior colliculus. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2010. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/ETD-UT-2010-12-2065.

Council of Science Editors:

Li, Na 1O2. Binaural mechanism revealed with in vivo whole cell patch clamp recordings in the inferior colliculus. [Doctoral Dissertation]. University of Texas – Austin; 2010. Available from: http://hdl.handle.net/2152/ETD-UT-2010-12-2065

University of Texas – Austin

15. Ramachandra, Vorani Sashrika. Dopamine responses in the ventral straitum contribute to ethanol preference and consumption and, mu opioid receptors do not mediate ethanol stimulated dopamine release.

Degree: PhD, Pharmacy, 2010, University of Texas – Austin

URL: http://hdl.handle.net/2152/ETD-UT-2010-08-1698

► The goal of this dissertation was two fold: 1) To relate dopamine responses in the ventral striatum to ethanol preference and consumption, and 2) to… (more)

▼ The goal of this dissertation was two fold: 1) To relate dopamine responses in the ventral striatum to ethanol preference and consumption, and 2) to investigate the role of the mu opioid receptors in this ethanol induced dopamine release in the ventral striatum. First a two bottle choice experiment established that a substrain of C57BL/6 mice (C57BL/6NCrl) had significantly less preference for and consumption of ethanol than a second substrain of mouse based on the same background (C57BL6/J). The C57BL/6 strain has been extensively used in alcohol drinking studies and is well known for it’s propensity to consume alcohol over water. To determine if differences in ventral striatal dopamine response vii could contribute to this variability in drinking behavior, we characterized the dopamine response in both substrains of mice after intraperitoneal injections of 1.0, 2.0 or 3.0 g/kg ethanol or saline. We found that the acute intraperitoneal ethanol injections in naïve mice caused a significant elevation in dopamine in both substrains at all three doses with a significant difference between substrains at the two highest alcohol doses. Therefore, ethanol induced dopamine release in the ventral striatum may contribute to ethanol preference and consumption. Next, we investigated the effect of acute intraperitoneal ethanol injections on naïve mu opioid receptor knockout mice and in mice pretreated with a mu opioid receptor antagonist. The mice used were all established on the C57BL/6J background. We found that ventral striatal dopamine response was similar in these mice after 1.0, 2.0 and 3.0 g/kg intraperitoneal ethanol injections compared to appropriate controls. As both gene deletion and pharmacological blockade of the mu opioid receptor did not affect ethanol stimulated dopamine release, it points to the conclusion that this receptor may not play a significant role in ethanol induced ventral striatal dopamine release. Advisors/Committee Members: Gonzales, Rueben Anthony (advisor), Duvauchelle, Christine L. (committee member), Gore, Andrea C. (committee member), Bergeson, Susan (committee member), Morrisett, Richard A. (committee member), Ponomarev, Igor (committee member).

Subjects/Keywords: Dopamine; Ethanol; Ventral striatum; Mu opioid receptor; Alcoholism

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APA (6^th Edition):

Ramachandra, V. S. (2010). Dopamine responses in the ventral straitum contribute to ethanol preference and consumption and, mu opioid receptors do not mediate ethanol stimulated dopamine release. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/ETD-UT-2010-08-1698

Chicago Manual of Style (16^th Edition):

Ramachandra, Vorani Sashrika. “Dopamine responses in the ventral straitum contribute to ethanol preference and consumption and, mu opioid receptors do not mediate ethanol stimulated dopamine release.” 2010. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/ETD-UT-2010-08-1698.

MLA Handbook (7^th Edition):

Ramachandra, Vorani Sashrika. “Dopamine responses in the ventral straitum contribute to ethanol preference and consumption and, mu opioid receptors do not mediate ethanol stimulated dopamine release.” 2010. Web. 27 Feb 2021.

Vancouver:

Ramachandra VS. Dopamine responses in the ventral straitum contribute to ethanol preference and consumption and, mu opioid receptors do not mediate ethanol stimulated dopamine release. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2010. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/ETD-UT-2010-08-1698.

Council of Science Editors:

Ramachandra VS. Dopamine responses in the ventral straitum contribute to ethanol preference and consumption and, mu opioid receptors do not mediate ethanol stimulated dopamine release. [Doctoral Dissertation]. University of Texas – Austin; 2010. Available from: http://hdl.handle.net/2152/ETD-UT-2010-08-1698

University of Texas – Austin

16. Theile, Jonathan William. Mechanisms in ethanol modulation of GABA release onto dopaminergic neurons of the ventral tegmental area.

Degree: PhD, Cell and Molecular Biology, 2009, University of Texas – Austin

URL: http://hdl.handle.net/2152/ETD-UT-2009-12-491

► Activation of ventral tegmental area (VTA) dopaminergic (DA) neurons by ethanol has been implicated in the rewarding and reinforcing actions of ethanol. GABAergic transmission is… (more)

▼ Activation of ventral tegmental area (VTA) dopaminergic (DA) neurons by ethanol has been implicated in the rewarding and reinforcing actions of ethanol. GABAergic transmission is thought to play an important role in regulating the activity of DA neurons. While at most central synapses ethanol generally increases inhibitory synaptic transmission, no studies have explored the effect of acute ethanol on GABAergic transmission in the VTA. Here we investigated how ethanol modulates GABAergic transmission in the VTA in relation to the overall action of ethanol on VTA-DA neuron activity. We demonstrated that ethanol dose-dependently enhances action potential-dependent and -independent GABA release onto VTA-DA neurons. Utilizing whole-cell voltage clamp recording techniques, ethanol increased both spontaneous and miniature inhibitory postsynaptic current (s/mIPSC) frequency while having minimal effect on s/mIPSC amplitude. The ethanol enhancement in GABA release was independent of GABAB auto-receptor inhibition of release. Intra-terminal calcium levels regulate neurotransmitter release, thus we investigated how modulation of calcium levels would affect the ethanol-enhancement in GABA release. Ethanol enhanced mIPSC frequency in the presence of the voltage-gated calcium channel blockers, cadmium chloride and nicardipine. However, blockade of intracellular calcium stores with 2-APB and cyclopiazonic acid eliminated the ethanol-enhancement of mIPSC frequency. Intracellular calcium stores are regulated via Gq protein-coupled receptors such as the 5-HT2C receptor. 5-HT2C receptor activation robustly enhanced mIPSC frequency whereas blockade inhibited the ethanol-enhancement in mIPSC frequency. These observations suggest that increased calcium release from intracellular stores via 5-HT2C receptor activation is involved in the ethanol-enhancement of GABA release onto VTA-DA neurons. Utilizing cell-attached current-clamp recordings, we demonstrated that the ethanol-enhancement of VTA-DA neuron activity is modulated by the concurrent enhancement in GABA release. Blockade and activation of GABAA receptors enhanced and reversed, respectively, the stimulatory effect of ethanol on VTA-DA neurons. Mu-opioid receptors (MORs) on GABAergic interneurons have been demonstrated to modulate both basal and ethanol-enhanced VTA-DA activity in vivo, though we failed to demonstrate such an effect in vitro. Overall, the results of this study suggest that the 5-HT2C receptor and intra-terminal calcium-dependent ethanol enhancement in GABA release acts to regulate the overall stimulatory effect of ethanol on VTA-DA activity. Advisors/Committee Members: Morrisett, Richard A. (advisor), Gonzales, Rueben A. (committee member), Morikawa, Hitoshi (committee member), Mayfield, R. Dayne (Roy Dayne), 1958- (committee member), Mihic, S. J. (committee member).

Subjects/Keywords: Midbrain; Reward; Alcohol; GABA; Dopaminergic

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Theile, J. W. (2009). Mechanisms in ethanol modulation of GABA release onto dopaminergic neurons of the ventral tegmental area. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/ETD-UT-2009-12-491

Chicago Manual of Style (16^th Edition):

Theile, Jonathan William. “Mechanisms in ethanol modulation of GABA release onto dopaminergic neurons of the ventral tegmental area.” 2009. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/ETD-UT-2009-12-491.

MLA Handbook (7^th Edition):

Theile, Jonathan William. “Mechanisms in ethanol modulation of GABA release onto dopaminergic neurons of the ventral tegmental area.” 2009. Web. 27 Feb 2021.

Vancouver:

Theile JW. Mechanisms in ethanol modulation of GABA release onto dopaminergic neurons of the ventral tegmental area. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2009. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/ETD-UT-2009-12-491.

Council of Science Editors:

Theile JW. Mechanisms in ethanol modulation of GABA release onto dopaminergic neurons of the ventral tegmental area. [Doctoral Dissertation]. University of Texas – Austin; 2009. Available from: http://hdl.handle.net/2152/ETD-UT-2009-12-491

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